Mechanism behind blood clots

Scientists using mice believe they have identified the mechanism which determines whether fatty deposits in the arteries are harmless or potentially fatal.

Fatty deposits in the arteries, called plaques, build up from the teenage years onwards. They are normal, and mostly harmless. However, a small percentage have the potential to burst, leaking their contents into the blood stream. This can restrict blood flow, and lead to clots which prevent blood flow altogether.

The team discovered that the inner core of the plaques contained dead cells. They believed that a substance released by these cells was responsible for weakening the surface of the plaque, leaving it more vulnerable to rupture. The aim of the researchers was to identify what causes these dead cells to build up in the plaques.

A gene called CHOP was thought to be a good candidate, as it plays a crucial role in cell death. The team therefore engineered ‘knockout’ mice (that did not express the CHOP gene), and compared the effect of a high-fat diet on them and on normal mice expressing the gene.

The mice without the CHOP gene tended to produce smaller plaques which were less susceptible to rupture. So the CHOP gene is probably involved in this process and provides a potential target for therapy. Future treatments could focus on preventing the harmless plaques in young people from becoming dangerous, or soothing those that are susceptible to rupture as the body ages.